Natural Killer Group 2D (NKG2D) is a member of the NKG2 family of HLA class I C-type lectin receptors and is expressed as a homodimer by natural killer (NK) cells (Burgess, et al. (2008) Immunol. Res. 40:18-34; Jonjic, et al. (2008) Eur. J. Immunol. 38:2927-68) and cytotoxic lymphocytes (Wrobel, et al. (2007) Scand. J. Immunol. 66:320-28; Saez-Borderias, et al. (2006) Eur. J. Immunol. 36:3198-06). The ligands for NKG2D are induced-self proteins that are absent or present at very low levels on the surface of normal cells, but can be expressed in increased amounts in infected, transformed, senescent, and stressed cells, and include the human major histocompatibility complex class I chain-related gene A (MICA) and MICB ligands (Mendoza-Rincon (2007) In Advances in Cancer Research at UNAM, Mas-Oliva, et al. eds. Mexico City, Manual Moderno, pg. 127-135), which are stress-induced molecules often expressed by various tumors, including those of epithelial origin (Paschen, et al. (2009) Clin. Cancer Res. 15:5208-15; Unni, et al. (2008) Proc. Natl. Acad Sci. USA 105:1686-91) and leukemias (Kato, et al. (2007) Leukemia 21:2103-08), as well as by virus-infected cells (Chalupny, et al. (2006) Biochem. Biophys. Res. Commun. 346:175-81; Tosh, et al. (2006) Hum. Mol. Genet. 15:2880-87). The recognition of the MICA and MICB ligands on tumor cells by the NKG2D receptor, found on NK cells, induces the cytotoxic activity of NK cells (Santoni, et al. (2007) Am. J. Reprod Immunol. 58:280-88) and the subsequent lysis of their tumor targets (Papazahariadou, et al. (2007) Int. J. Biol. Markers 22:144-53). The secretion of MICA and MICB by cancer cells has been suggested as a mechanism for tumor cell immune escape through the saturation of NKG2D receptors on cytotoxic cells (Salih, et al. (2006) Hum. Immunol. 67:188-95; Marten, et al. (2006) Int. J. Cancer 119:2359-65), thus abrogating their ability to recognize tumor cells. In fact, higher amounts of these molecules were found in the sera of human cancer patients compared to healthy individuals (Salih, et al. (2008) Front. Biosci. 4A:2041-45), and a direct correlation was found between increased serum concentrations of these molecules and tumor stage (Holdenrieder, et al. (2006) Cancer Immunol. Immunother. 55:1584-89). Patients responding to immunotherapy have been shown to mount antibody responses targeting MICA, which permits re-engagement of immunity (May, et al. (2012) J. Clin. Oncol. 30(suppl.):abstract 2502). Moreover, antibodies targeting MICA and MICB have been shown to block the MICA/NKG2D interaction and mediate complement-dependent cytotoxicity (CDC) and antibody-dependent cell cytotoxicity (ADCC) toward MICA expressing cells (Bonnafous, et al. (2013) J. Immuno Ther. Cancer 1(Suppl 1):P41). See also, WO 2014/144791 and WO 2013/117647.